EED Antibody

1. we present a patient with a clinical diagnosis of Weaver syndrome and novel de novo sequence variant in EED. Our observation together with previous reports [2, 3, 5] suggests that EED gene testing is warranted in patients with the overgrowth syndrome features and suspicion of Weaver syndrome with normal results for EZH2 gene sequencing. PMID:29410511
2. Data suggest the polycomb repressive complex 2 subunits EZH2, SUZ12, and EED protein axis as promising therapeutic target for treating sarcoma. PMID:29415665
3. These findings support that Weaver syndrome is a disorder with locus heterogeneity and can be due to pathogenic variants in either EZH2 or EED. This case highlights the utility of exome sequencing as a clinical diagnostic tool for novel gene discovery as well as the importance of re-examination of exome data as new information about gene-disease associations becomes available. PMID:27868325
4. we have found two unrelated families of different ethnicities, with a similar rare phenotype, both associated with de novo mutations in this member of the PRC2 complex, we are confident that EED is indeed a novel overgrowth gene. PMID:27193220
5. Mutations of SUZ12 and EED are reported to have tumor suppressive functions. (Review) PMID:27000413
6. These results suggest that the SNPs of the EED gene might not be associated with susceptibility to CRC. PMID:23709348
7. An integral role for EED as an epigenetic exchange factor coordinating the activities of PRC1 and 2, is reported. PMID:24457600
8. Data show that overall enhancer of zeste 2 (EZH2), embryonic ectoderm development (EED) and suppressor of zeste 12 homolog (SUZ12) expression in the colorectal cancer (CRC) tissues was significantly increased than in the non-cancerous tissue. PMID:25326896
9. EED, a component of Polycomb repressive complex-2 (PRC2) that catalyzes methylation of lysine 27 of histone H3 (H3K27), was involved in epithelial-mesenchymal transition (EMT) of cancer cells induced by Transforming Growth Factor-beta (TGF-beta). PMID:25264103
10. Polycomb repressive complex 2 is recurrently inactivated through EED or SUZ12 loss in malignant peripheral nerve sheath tumors. PMID:25240281
11. EZH2-EED is necessary and sufficient for binding to the lncRNA HOTAIR. PMID:24320048
12. Although inactivating mutations in PRC2-encoding genes EZH2, EED, and SUZ12 are present in T-cell acute lymphoblastic leukemia and in myeloid malignancies, gain-of-function mutations in EZH2 are frequently observed in B-cell lymphoma. PMID:23982173
13. EED mutants impair polycomb repressive complex 2 and is associated with myelodysplastic syndrome and related neoplasms PMID:22733077
14. Promoter polymorphism of the EED gene is associated with the susceptibility to ulcerative colitis. PMID:22271413
15. Genetic defects in PRC2 components other than EZH2 are not common in myeloid malignancies. PMID:22308284
16. The authors found that Sox2 and Eed positively regulate each other's expression and contribute to the maintenance of self-renewal in embryonic stem cells by controlling histone methylation and acetylation. PMID:21540835
17. molecular basis of EED-methyllysine recognition, and the biochemical characterization of how the activity of a histone methyltransferase is oppositely regulated by two histone marks. PMID:20974918
18. histone modification including PRC2-mediated repressive histone marker H3K27me3 and active histone marker acH4 may involve in CD11b transcription during HL-60 leukemia cells reprogramming to terminal differentiation[polycomb repressive complex 2 ] PMID:19578722
19. EED is a nuclear factor and repressor of transcription and is recruited to the plasma membrane by HIV-1 nef PMID:14759364
20. EED exerted an antiviral activity at the late stage of HIV-1 replication, which included genomic RNA packaging and virus assembly, resulting possibly from a mistrafficking of viral genomic RNA (gRNA) or gRNA/Gag complex. PMID:17547741
21. NIPP1 is present in a complex with EED and EZH2 in vivo and has distinct binding sites for these proteins. PMID:17804093
22. Identification of antibody-, MA-, IN- and EZH2-binding sites at EED's surface provides a global picture of the immunogenic and protein-protein interacting regions in the EED C-terminal domain, organized as a seven-bladed beta-propeller protein. PMID:18302803
23. the carboxy-terminal domain of EED specifically binds to histone tails carrying trimethyl-lysine residues associated with repressive chromatin marks, and this leads to the allosteric activation of the methyltransferase activity of PRC2. PMID:19767730

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HGNC: 3188

UNIGENE: Hs.503510

KEGG: hsa:8726

STRING: 9606.ENSP00000263360

OMIM: 605984